Introduction

Neurology has long been defined by the classification of loss. Agnosia - from the Greek "a-gnosis," meaning not knowing - describes patients who perceive without recognition. Apraxia - "a-praxis," meaning not doing - describes patients who command strength without skill. Since the seminal descriptions by Lissauer on visual agnosia and Liepmann on apraxia, these terms have proliferated into an extensive taxonomy. Yet, the literature often fragments them by modality, producing lists of syndromes rather than a unifying schema.

In contemporary neuroscience, however, the nervous system is increasingly understood as a distributed network. Failures of recognition and praxis occur in every sensory and motor domain. Each represents a specific point of breakdown between sensation, knowledge, intention, and action. When mapped onto the homunculus - the cortical representation of the body - they form a coherent chart of how "unknowing" manifests across the brain.

This review reconstructs that chart.

Visual Recognition Disorders

Vision has yielded the richest catalog of agnosias. Apperceptive agnosia reflects an inability to integrate visual features into coherent percepts despite intact acuity. Associative agnosia preserves perception but severs links to semantic knowledge.

More specialized syndromes populate this domain:

• Prosopagnosia, the inability to recognize familiar faces, localizes to the fusiform face area.
• Pure alexia, or visual word-form agnosia, isolates reading from writing.
• Color agnosia and cerebral achromatopsia dissociate color naming from color perception.
• Akinetopsia selectively abolishes motion perception.
• Simultanagnosia, the inability to perceive multiple objects at once, defines Bálint's syndrome.
• Topographical agnosia, including landmark agnosia and heading disorientation, reflects failures in spatial scene recognition.

These conditions illustrate the vulnerability of visual cognition not to blindness, but to meaninglessness.

Auditory Recognition Disorders

Auditory agnosias mirror visual forms. Pure word deafness interrupts spoken language comprehension despite intact hearing. Environmental sound agnosia erases recognition of non-speech sounds. Phonagnosia removes the familiarity of voices. Amusia disables melodic or rhythmic processing. Prosodic agnosia strips speech of its emotional inflection.

Lesions in superior temporal and right hemispheric cortices underscore the modularity of auditory recognition.

Tactile and Somatosensory Disorders

The tactile system also fractures: astereognosis impairs object identification by touch; amorhagnosia and ahylognosia selectively abolish shape or texture knowledge; agraphesthesia prevents recognition of letters traced on the skin; finger agnosia, a core element of Gerstmann's syndrome, disrupts body part identification.

Olfactory and Gustatory Disorders

Though less common, olfactory agnosia and gustatory agnosia demonstrate that chemical senses, too, can lose their semantic linkage. These syndromes often arise after orbitofrontal or mesial temporal injury, implicating limbic-frontal circuits.

Body-Schema and Ownership Disorders

Perhaps the most philosophically striking are disorders of self-awareness. Anosognosia, described by Babinski in 1914, denotes unawareness of deficit, most often hemiplegia. Asomatognosia and hemiasomatognosia erase body parts from awareness. Somatoparaphrenia projects alien ownership onto one's limb. Autotopagnosia disrupts localization of body parts. Together, these syndromes emphasize that the self is neurologically constructed and vulnerable.

Attention and Neglect

Right hemisphere lesions yield profound attentional "apraxias." Hemispatial neglect erases contralesional space from awareness. Extinction eliminates perception of bilateral stimuli. Allochiria and achiria mislocalize sensation to the wrong side. These disorders highlight attention as an active, motor-sensory function mapped onto the homunculus.

Apraxias of Action

Parallel to agnosia, apraxia represents the loss of action grammar. Ideomotor apraxia disconnects intention from movement; ideational apraxia abolishes sequencing; conceptual apraxia disrupts tool knowledge; limb-kinetic apraxia removes precision; oral/buccofacial apraxia impairs orofacial gestures; dressing apraxia and constructional apraxia impair clothing orientation and spatial construction.

Language and Symbolic Processing

Language produces symbolic agnosias: alexia and agraphia; acalculia; anomia; color anomia. These demonstrate that symbolic cognition is embodied, subject to the same disconnections as sensory knowledge.

Disconnection and Composite Syndromes

Corpus callosum lesions yield tactile disconnection and alexia without agraphia. Composite syndromes include Gerstmann's syndrome, Bálint's syndrome, and the cerebellar cognitive-affective syndrome. These illustrate that cognition is not housed in modules but in networks, vulnerable at their points of connection.

Discussion

Taken together, these syndromes constitute a taxonomy of "unknowing." Each sensory and motor domain harbors its own agnosias and apraxias, each with preferential hemispheric vulnerabilities. When organized across the homunculus, the result is not a random catalog but a structured framework of potential failures at the junctions of perception, knowledge, intention, and execution.

Clinically, this framework enhances diagnostic precision and lesion localization. Educationally, it provides a coherent schema for trainees. Theoretically, it underscores that cognition is not just the accumulation of inputs and outputs but the fragile continuity between them.

Conclusion

Agnosias, apraxias, neglects, symbolic deficits, and body-awareness syndromes together represent a coherent family of disorders: the failure to know, to act, to attend, or to own. By charting these across the homunculus, we expose the architecture of human cognition in both its strengths and vulnerabilities.